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Study · Animal study (in vivo) · mouse · 2020

5 results

Protective effects of SS-31 against SDHB suppression-mitochondrial dysfunction-EndMT axis-modulated CBT sclerosis and progression.

Tang H, Fang C, Xue S, Zhao G, Shi Z, Fu W, Zhang P, Tang X, Guo D

American journal of translational research15 Nov 2020Cited by 3 (Europe PMC)

PMID33312392 (opens in a new tab)PMCIDPMC7724343 (opens in a new tab)PepBankPUB-33312392
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study5

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In PDX mice with sclerosing carotid body tumor, SS‑31 treatment significantly retarded tumor progression.

    In plain wordsIn mice with transplanted carotid body tumors, SS‑31 slowed tumor progression.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseSclerosing carotid body tumor progression
    Study

    mousen: not reported in source

    Patient-derived xenograft (PDX) model of sclerosing carotid body tumor
    Comparator
    Sclerosing carotid body tumor without SS-31
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    And treating with SS-31 could significantly retard SCBT progression by rescuing the mitochondrial dysfunction-induced EndMT.
    1 context sentence
    Summary · context
    In patient-derived xenograft (PDX) mice models of CBT, we also observed increased tumor growth speed and extent of EndMT, mitochondrial dysfunction, and metabolic switch in sclerosing carotid body tumor (SCBT) group than in conventional carotid body tumor (CCBT) group.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In PDX mice with sclerosing carotid body tumor, SS‑31 treatment rescued the mitochondrial dysfunction-induced EndMT.

    In plain wordsIn mice with transplanted carotid body tumors, SS‑31 reversed a cell-change process (EndMT) linked to mitochondrial problems.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseEndMT in sclerosing carotid body tumor
    Study

    mousen: not reported in source

    Patient-derived xenograft (PDX) model of sclerosing carotid body tumor
    Comparator
    Sclerosing carotid body tumor without SS-31
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    And treating with SS-31 could significantly retard SCBT progression by rescuing the mitochondrial dysfunction-induced EndMT.
    1 context sentence
    Summary · context
    In patient-derived xenograft (PDX) mice models of CBT, we also observed increased tumor growth speed and extent of EndMT, mitochondrial dysfunction, and metabolic switch in sclerosing carotid body tumor (SCBT) group than in conventional carotid body tumor (CCBT) group.
  3. 03LabIn vitro (cells)Mechanism

    In HUVECs with SDHB knockdown and hypoxia, SS‑31 treatment attenuated endothelial-mesenchymal transition (EndMT).

    In plain wordsIn lab tests on endothelial cells with SDHB knockdown and low oxygen, SS‑31 reduced a cell-change process called EndMT.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseEndMT in SDHB-knockdown HUVECs
    Study

    n: not reported in source

    HUVECs with SDHB knockdown and hypoxia
    Outcome group
    Tumor growth · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human umbilical vein endothelial cells (HUVECs), SDHB KD aggravated hypoxia-induced EndMT, mitochondrial dysfunction and metabolic switch, while SS-31 treatment could significantly attenuate these changes caused by SDHB KD and hypoxia.
  4. 04LabIn vitro (cells)Mechanism

    In HUVECs with SDHB knockdown and hypoxia, SS‑31 treatment attenuated mitochondrial dysfunction.

    In plain wordsIn lab tests on endothelial cells with SDHB knockdown and low oxygen, SS‑31 reduced mitochondrial dysfunction.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMitochondrial dysfunction in SDHB-knockdown HUVECs
    Study

    n: not reported in source

    HUVECs with SDHB knockdown and hypoxia
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human umbilical vein endothelial cells (HUVECs), SDHB KD aggravated hypoxia-induced EndMT, mitochondrial dysfunction and metabolic switch, while SS-31 treatment could significantly attenuate these changes caused by SDHB KD and hypoxia.
  5. 05LabIn vitro (cells)Mechanism

    In HUVECs with SDHB knockdown and hypoxia, SS‑31 treatment attenuated the metabolic switch.

    In plain wordsIn lab tests on endothelial cells with SDHB knockdown and low oxygen, SS‑31 reduced a shift in cell metabolism.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseMetabolic switch in SDHB-knockdown HUVECs
    Study

    n: not reported in source

    HUVECs with SDHB knockdown and hypoxia
    Outcome group
    Mitochondrial function · Cancer
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human umbilical vein endothelial cells (HUVECs), SDHB KD aggravated hypoxia-induced EndMT, mitochondrial dysfunction and metabolic switch, while SS-31 treatment could significantly attenuate these changes caused by SDHB KD and hypoxia.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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